Dynamics of tissue oxygenation in isolated rabbit heart as measured with near-infrared spectroscopy

We investigated the role of myoglobin (Mb) in supplying O2 to mitochondria during transitions in cardiac workload. Isovolumic rabbit hearts ( n = 7) were perfused retrogradely with hemoglobin-free Tyrode solution at 37°C. Coronary venous O2 tension was measured polarographically, and tissue oxygenation was measured with two-wavelength near-infrared spectroscopy (NIRS), both at a time resolution of ∼2 s. During transitions to anoxia, 68 ± 2% (SE) of the NIRS signal was due to Mb and the rest to cytochrome oxidase. For heart rate steps from 120 to 190 or 220 beats/min, the NIRS signal decreased significantly by 6.9 ± 1.3 or 11.1 ± 2.1% of the full scale, respectively, with response times of 11.0 ± 0.8 or 9.1 ± 0.5 s, respectively. The response time of end-capillary O2 concentration ([O2]), estimated from the venous [O2], was 8.6 ± 0.8 s for 190 beats/min ( P< 0.05 vs. NIRS time) or 8.5 ± 0.9 s for 220 beats/min ( P > 0.05). The mean response times of mitochondrial O2 consumption (V˙o 2) were 3.7 ± 0.7 and 3.6 ± 0.6 s, respectively. The deoxygenation of oxymyoglobin (MbO2) accounted for only 12–13% of the total decrease in tissue O2, with the rest being physically dissolved O2. During 11% reductions in perfusion flow at 220 beats/min, Mb was 1.5 ± 0.4% deoxygenated ( P < 0.05), despite the high venous [Formula: see text] of 377 ± 17 mmHg, indicating metabolism-perfusion mismatch. We conclude that the contribution of MbO2 to the increase of V˙o 2 during heart rate steps in saline-perfused hearts was small and slow compared with that of physically dissolved O2.